Quantitation and kinetics of blood monocyte migration to acute inflammatory reactions, and IL-1 alpha, tumor necrosis factor-alpha, and IFN-gamma.
Quantitation and kinetics of blood monocyte migration to acute inflammatory reactions, and IL-1 alpha, tumor necrosis factor-alpha, and IFN-gamma.
复制标题
血液单核细胞迁移至急性炎症反应以及 IL-1 α、肿瘤坏死因子-α 和 IFN-γ 的定量和动力学。
DOI：
10.4049/jimmunol.151.4.2105
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发表时间：
1993
影响因子：
4.4
通讯作者：
T. Issekutz
中科院分区：
文献类型：
--
作者：
A. Issekutz;T. Issekutz
单核细胞从血液中迁移到急性炎症反应中，在那里它们分化成巨噬细胞，并在12至24小时后成为炎性浸润的主要组织学特征。单核细胞迁移到这些反应的定量一直是困难的。本报告采用了一种新的技术组合，从大鼠血液中分离高度纯化的单核细胞，并表明这些细胞具有正常的t1/2为26小时，静脉注射后有效地迁移到皮肤急性炎症部位。51 Cr标记的单核细胞在迟发型超敏反应中积累，并在注射灭活大肠杆菌、LPS、聚肌苷：胞嘧啶、酵母聚糖激活血清（ZAS）（C5 adesArg的来源）和细胞因子IL-1 α、TNF-α和IFN-γ的部位积累。放射性标记的单核细胞和中性粒细胞均迅速迁移到E.大肠杆菌、LPS、ZAS、IL-1 α和TNF-α，细胞积累在2 h时大幅增加。所有五种刺激物在3至4小时时，神经细胞迁移迅速下降至检测不到的水平，单核细胞迁移至ZAS和IL-1 α的水平也在此时下降。与之相反，E.大肠杆菌，LPS和TNF-α引起单核细胞持续迁移5至6小时，中性粒细胞已经停止积累后很长时间。皮内IFN-γ没有招募中性粒细胞，但刺激单核细胞迁移1至6小时。LPS、TNF-α和IFN-γ的组合协同增强单核细胞募集的晚期（> 5小时）而非早期。总之，从大鼠血液中分离的纯化单核细胞可用于定量体内单核细胞迁移，这些细胞迅速迁移至皮肤炎症，并响应趋化因子IL-1 α、TNF-α和IFN-γ，其初始动力学与中性粒细胞相似。然而，单核细胞选择性机制是由IFN-γ诱导的，并且似乎也参与了单核细胞向TNF-α、LPS和E.杆菌
Monocytes migrate from the blood into acute inflammatory reactions, where they differentiate into macrophages, and after 12 to 24 h become the predominant histologic feature of the inflammatory infiltrate. The quantitation of monocyte migration into these reactions has been difficult. This report employs a novel combination of techniques to isolate highly purified monocytes from the blood of rats, and shows that these cells have a normal t1/2 of 26 h and migrate efficiently after i.v. injection into cutaneous acute inflammatory sites. Monocytes labeled with 51Cr accumulated in delayed-type hypersensitivity reactions, and sites injected with killed Escherichia coli, LPS, poly-inosine: cytosine, zymosan-activated serum (ZAS), a source of C5adesArg, and the cytokines IL-1 alpha, TNF-alpha, and IFN-gamma. Both radiolabeled monocytes and neutrophils migrated rapidly to E. coli, LPS, ZAS, IL-1 alpha, and TNF-alpha with a large increase in cell accumulation by 2 h. Neutrophil migration declined rapidly to undetectable levels by 3 to 4 h to all five stimuli, and monocyte migration to ZAS and IL-1 alpha also declined by this time. In contrast, E. coli, LPS, and TNF-alpha caused a sustained migration of monocytes for 5 to 6 h, long after neutrophils had stopped accumulating. Intradermal IFN-gamma did not recruit neutrophils but stimulated a prolonged monocyte migration from 1 to 6 h. Combinations of LPS, TNF-alpha, and IFN-gamma synergistically enhanced the late (> 5 h) but not the early phase of monocyte recruitment. In conclusion, purified monocytes isolated from rat blood can be used to quantify monocyte migration in vivo, and these cells migrate rapidly to cutaneous inflammation and in response to chemotactic factors, IL-1 alpha, TNF-alpha, and IFN-gamma, with initial kinetics similar to those of neutrophils. However, monocyte-selective mechanisms are induced by IFN-gamma and also appear to be involved in prolonged monocyte migration to TNF-alpha, LPS, and E. coli.